Dr. Mangesh H Tiwaskar: A Case of Drug-Resistant Hypertension

CASE OVERVIEW

A 51 year old man was referred for elevated blood pressure to Dr. Mangesh H Tiwaskar. He was 178 cm in height, weighed 94.5 kg and had lost 3 kg in the past 2 months. He was a known case of type 2 diabetes for 5 years and hypertension for 12 years. He frequently complained of fatigue and dry mouth and had no known history of hypertension target-organ damage. On enquiring about family’s medical history, it revealed no remarkable history other than hypertension in both parents. On examination, his seated BP was 156/90 mmHg in the left arm and 158/90 mmHg in the right arm, no difference in standing BP, and had heart rate of 70 beats/min.

Patient was on following medication

1.   Hydrochlorothiazide 25mg,
2.  Valsartan 160mg,
3.  Diltiazem (long acting) 300mg,
4.  Clonidine 0.2mg,
5.  Metoprolol (long acting) 100mg,
6.  Simvastatin 40mg,
7.  TriCor 145mg,
8.  Metformin 1000mgDIAGNOSIS

The patient was advised to follow these seven basic steps used to pursue drug-resistant hypertension in an office setting.

1.  Confirm treatment resistance
   To find if there are any differences in the office-based BP and when the patient leaves office. This step is important as it helps to differentiate between white coat or office hypertension and resistant hypertension
2.  Exclude pseudoresistance
   Pseudoresistance can arises due to technical errors such as inadequately matched cuffs, no rest for 5 min prior to BP measurement, or digit bias.
3.  Identify and reverse lifestyle factors
   Lifestyle factor such as excess sodium intake or excess body weight contributes to drug-resistant hypertension. A low-salt diet shows 23/9-mmHg (systolic over diastolic) difference in BP, whereas, an average weight loss of 8 kg decreases BP by 6 to 10mmHg. Therefore, making it essential to identify and reverse lifestyle factors.
4.  Discontinue interfering substances.
   Substances such as NSAIDs, over-the-counter remedies, alcohol and strength/endurance enhancers interfere with the functioning of anti-hypertensive medications. Therefore, patients should be advised to stop.
5.  Screen for secondary hypertension.
   To screen and check for other possible causes of elevated blood pressure such as adrenal, renal, or the other few possibilities.
6.  Pharmacological treatment.
   To employ a regimen of antihypertensive medication that is complementary and not overlapping in action.
7.  Refer to a specialist.
   Our patient’s out-of-the-office BP were slightly lower than office BP, however, both values were above 150 mmHg. While performing his BP measurements at home, he followed the directions correctly. On enquiring about his eating habits, he was well aware of his sodium intake and made sure to read food labels carefully. He took his medication regularly. On clinical examination, his CT angiogram was negative both for renal vascular disease and for abnormalities in the adrenal glands. His metanephrine assay was in the normal range. His plasma renin: 0.10 ng/ml per h (normal 1.5 to 3.5 ng/ml per h), and aldosterone: 8 ng/dl (normal 3 to 15 ng/dl). The renin activity was suppressed, but the aldosterone concentration was in the middle of the normal range.It is defined that a patient qualifies for drug-resistant hypertension when a person takes three or more antihypertensive drugs, one of which is a diuretic, and has a BP of more than 140/90 mmHg. Simultaneously, even with good diuretic therapy, an element of volume excess may persist in the drug-resistant hypertensive. The low renin activity supports this possibility.

Our patient qualified for drug-resistant hypertension. As he was on five anti-hypertensive medicine with BP of 156 to 158/90 – mmHg BP and had low renin activity.

TREATMENT

With the renin and aldosterone data, patients was discussed about adding a mineralocorticoid antagonist. After discussing the pros and cons of mineralocorticoid antagonist (spironolactone and eplerenone), drug eplerenone was added. The reason for drug choice was based on

1.  According to ASCOT, the addition of an aldosterone antagonist reduces BP by 22/10 mmHg.
2.  Low renin activity in the patient suggested a sodium surfeit.
3.  Patient was advised to monitor potassium and creatinine levels.

RESULT

Course of BP response to patient.

“Redo diltiazem” means that the dose had to be titrated back to a former level.
D/C, discontinue; SBP, systolic BP; DBP, diastolic BP.

During the follow up laboratory check up it was notes that the effect of aldosterone antagonism was not evident in the first few weeks of treatment. There was a slight increase in creatinine (from 1.3 mg/dL up to 1.5 mg/dL). However, no change in potassium values as well as the blood sugar control.